Recent advance in mouse genetics has identified novel and crucial genes of embryonic heart development. However, congenital heart diseases (CHDs) are induced not only by genetic disorders but also by environmental factors such as maternal intake of drugs and alcohol, and transplacental viral infections. Maternal administration of retinoic acid (RA), one of vitamin A derivatives, has been reported to induce CHDs in mouse embryos. We established here much more wider spectrums of CHD models than previously reported by modifying the administration of RA. RA treatment at E6.5–6.75 induced impaired right–left axis and cardiac inflow tracts such as right or left isomerism heart with common atrioventricular canal and transposition of great arteries, and hypoplastic left heart syndrome with aortic and mitral atresia. E8.5 induced impaired rotation of outflow tracts such as transposition of great arteries or double outlet right ventricle. E9.0–9.5 induced impaired formation of the secondary heart field or inhibited migration of neural crest cells such as persistent truncus arteriosus, aorto-pulmonary window, interrupted aortic arch, tetralogy of Fallot, non-confluent pulmonary arteries, aberrant right subclavian artery, and right aortic arch, hypoplastic thymus, cleft palate, which are similar to human DiGeorge syndrome. It is very interesting that the administration of a single drug, RA, at various stage of embryonic development induced wide range of heart defects very similar to human CHDs. We are now trying to confirm critical and responsible genes for the inflow and the outflow tract morphogenesis by DNA microarray.